Pauci Immune Glomerulonephritis; A Late Complication of COVID-19 Infection

Abstract

Introduction: Coronavirus disease is a multi-organ disease caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS- CoV-2). Although acute kidney injury, collapsing glomerulopathy and thrombotic micro-angiopathy have been frequently attributed to COVID-19, pauci-immune glomerulonephritis (GN) has rarely been described [1]. Here we report a case of pauci-immune GN associated with SARS-CoV-2. Case Presentation: A 53 years old female with hypertension, diabetes mellitus, hepatitis C (treated 6 years ago), and recent covid-19 pneumonia (3 months ago), presented with dysuria, nausea, and vomiting. She denied fever, flank pain, and hematuria. The laboratory workup showed elevated blood urea nitrogen BUN 82 mg/dl and creatinine Cr 9.8 mg/dl (baseline creatinine was 0.9 mg/dl three months ago). Urinalysis showed proteinuria >1000 mg/dl and urine protein creatinine ratio of 5.3 (normal < 0.1), concerning for glomerulonephritis. Serological evaluation for glomerular disease showed normal complements C3 and C4, normal titers of anti-neutrophil cytoplasmic antibodies including p-ANCA, c-ANCA, atypical ANCA, and cryoglobulins. Screening for Hepatitis B and Hepatitis C was negative. The remainder of the autoimmune workup was unremarkable including Rheumatoid factor, Anti CCP antibodies (Ab), Anti Ribo-nucleoprotein Ab, and Anti Glomerular basement membrane antibodies. Coronavirus PCR was negative and qualitative IgG was reactive. CT chest showed idiopathic pulmonary fibrosis (IPF) and resolving ground glass opacities from prior coronavirus infection. CT abdomen and pelvis was unremarkable for obstructive uropathy. The renal biopsy showed pauci-immune focal sclerosis with 20% fibro-cellular crescents diagnostic for pauci-immune glomerulonephritis. The patient was treated for pauci-immune glomerulonephritis with pulse-dose intravenous steroids (methylprednisolone) followed by oral prednisone and rituximab. The renal functions improved dramatically (on day 15, her creatinine down-trended to 4 mg/dl from 9mg/dl on admission). She did not require intermittent hemodialysis and was discharged on day 15 with outpatient follow up. Discussion: The mechanisms of acute kidney injury in COVID-19 include renal hypoperfusion, endothelial dysfunction, micro-thrombi, and cytopathic effects of SARS-CoV-2 towards renal tubules and glomeruli. Due to a lack of scientific evidence related to coronavirus disease, the management of glomerulopathy is challenging. The existing literature favors the use of anti-viral therapy with immunosuppressive agents without the concern of worsening infection [2].